Resp Flashcards
Chronic dyspnea DDx (10)
Pulmonary causes include: Chronic obstructive pulmonary disease (COPD) Pleural effusions Interstitial lung disease Pulmonary hypertension Neuromuscular disease Severe kyphoscoliosis
Cardiac causes include:
Heart failure (e.g., related to decreased cardiac output or valvular disease)
Restrictive pericarditis
Other causes include:
Chronic anemia
Severe obesity
Acute dyspnea DDx (15)
Pulmonary causes include: Asthma Bronchitis Pneumonia Pneumothorax Pulmonary embolism Large airway obstruction (aspiration of foreign body, epiglottitis) Airway irritants (smoke, aerosols)
Cardiac causes include:
Heart failure (including failure related to an acute myocardial infarction)
Tamponade
Other causes include: Hemorrhage Hemolysis Carbon monoxide poisoning Psychogenic (hyperventilation syndrome, panic attack) High altitude Exercise
Acute dyspnea + each of the following DDx: Cough (4) Sputum production (2) Pleuritic chest pain (3) Visceral chest pain, angina (1) Hemoptysis (3)
Cough (bronchitis, asthma, pneumonia, airway irritation)
Sputum production (bronchitis, pneumonia)
Pleuritic chest pain (spontaneous pneumothorax, pulmonary embolus, pneumonia)
Visceral chest pain, angina (heart failure)
Hemoptysis (pulmonary embolus, bronchitis, pneumonia)
For each Disease: FVC, FEV1, FEV1%, TLC, RV, DLCO
Emphysema
Chronic bronchitis
Asthma (active flare of disease)
Interstitial lung disease
Extrapulmonary restriction (e.g., kyphoscoliosis)
Heart failure (early, increased blood flow)
Heart failure (late, with pulmonary edema)
Pulmonary embolus
Disease, FVC, FEV1, FEV1%, TLC, RV, DLCO
Emphysema ↓↓↓↑↑↓
Chronic bronchitis↓↓↓—↑—
Asthma (active flare of disease)↓↓↓—↑—/↑
Interstitial lung disease↓— —/↑↓↓↓
Extrapulmonary restriction (e.g., kyphoscoliosis)↓↓—↓—/↓—
Heart failure (early, increased blood flow) —————↑
Heart failure (late, with pulmonary edema) —————↓
Pulmonary embolus —————↓
Acute cough is most commonly due to _________(1) while chronic cough is most commonly due to ___________(4).
acute upper respiratory tract pathology (general viral infection)
secondary to chronic upper airway conditions (allergies, sinusitis), asthma, and gastroesophageal reflux disease.
Patient with cough: things to look for on physicals exam to help narrow DDx (10)
Sinus tenderness (sinusitis)
Conjunctival injection, rhinitis (URI)
Tympanic membrane erythema (otitis)
Oropharyngeal “cobblestoning” (chronic sinusitis)
Loose rhonchi (infection; i.e., bronchitis or pneumonia)
Consolidation (pneumonia)
Fine crackles (pulmonary edema)
Focal wheezing (local obstructing lesion; i.e., tumor or foreign body)
End-expiratory wheezing (obstructive airways disease; i.e., asthma/chronic obstructive pulmonary disease [COPD])
Nature of the cough itself (eg dry, irritant, nonproductive cough secondary to ACE inhibitors, or productive early morning cough encountered in chronic bronchitis).
Causes of cough due to: Upper Respiratory Infection (3) Lower Respiratory Infection (3) Environmental Pollutants (3) Mechanical Irritation (of upper or lower respiratory tract) (4) Chronic Inflammatory States (4) Drugs (2)
Upper Respiratory Infection (generally viral):
Pharyngitis
Sinusitis (via persistent nasal secretions into the pharynx—“postnasal drip”)
Tracheitis
Lower Respiratory Infection:
Bronchitis
Pneumonia
Tuberculosis
Environmental Pollutants:
Dust
Pollen, animal dander, and other allergens
Cigarette smoke
Mechanical Irritation (of upper or lower respiratory tract): Tumor Aortic aneurysm Cerumen Pulmonary edema
Chronic Inflammatory States: Asthma Chronic aspiration Gastroesophageal reflux disease Sarcoidosis
Drugs:
Angiotensin-converting enzyme (ACE) inhibitors
Psychogenic
Two major entities encompass COPD: what are they and how are they defined?
emphysema and chronic bronchitis.
Both result in airflow obstruction that is not fully reversible.
Chronic bronchitis is defined as excess tracheobronchial mucus production resulting in a productive cough that occurs for at least 3 months a year for 2 or more consecutive years. (Clinical Dx)
Emphysema is defined as abnormal dilatation of terminal airspaces with destruction of the alveolar septa. (Pathological Dx)
Chronic bronchitis: Pathophysiology? Is there V/Q mismatch?
- distinctive hypertrophy and hyperplasia of the mucus-producing glands that line the airways.
- chronic mucosal and submucosal inflammation, intraluminal mucus plugging, and smooth muscle hypertrophy; more pronounced in most distal, smaller caliber airways.
- The loss of ventilation in regions distal to the airway obstruction results in ventilation/perfusion (V/Q) mismatches and hypoxia.
Emphysema: 2 types; what pattern and risk factors are associated with each? Is there V/Q mismatch?
- centrilobular emphysema: areas most affected are respiratory bronchioles and the central alveolar ducts. Assoc with cigarette smoking.
- panacinar emphysema: destruction throughout the acinus. Assoc with α1-antitrypsin deficiency
Destruction of airspace and blood vessels is equal; therefore, marked V/Q mismatch does not occur.
Physiologic changes that result from COPD: (5)
Decreased FEV1 (FEV1 dep on Airway diameter, Collapsibility of the airways, Elastic recoil of the lung parenchyma)
V/Q mismatches (generally shunt, i.e., blood flow to nonventilated areas, resulting in hypoxia)
Pulmonary hypertension (in part because of loss of blood vessels from alveolar destruction, but more important is vessel constriction caused by hypoxia)
Abnormal ventilatory responses (blunted response to hypercapnia and a reliance on hypoxic respiratory drive, generally seen in patients with chronic bronchitis)
Right heart failure (caused by long-standing pulmonary hypertension, so-called cor pulmonale)
What are blue bloaters and pink puffers?
Blue bloaters: patients with chronic bronchitis.
- comfortable at rest.
- Obesity and cyanosis, maybe peripheral edema.
- Lung examination is usually resonant, often with coarse rhonchi and wheezes.
- clubbing is rare and, if present, is suggestive of an additional condition (eg lung cancer).
Pink puffers: pt with emphysema
- dyspnea at rest
- appears thin without cyanosis.
- markedly prolonged expiratory phase, often through pursed lips.
- Hypertrophy of accessory muscles in neck, and retraction of intercostal muscles with inspiration.
- lung exam: hyperresonant, with decrease in breath sounds, an increased anteroposterior chest diameter, and lowered diaphragms.
- distant heart sounds, absent signs of right heart overload.
Spirometric Classification of COPD Severity Based on Post-Bronchodilator FEV1 (staging)
Stage I: Mild
FEV1/FVC <50% predicted plus chronic respiratory failure
Bronchodilator therapy can alleviate symptoms significantly in some COPD patients. Agents fall into three classes:
Anticholinergics (e.g., ipratropium, tiotropium)
β-Adrenergic agonists (e.g., albuterol, salmeterol)
Methylxanthines (e.g., theophylline)
**Inhaled anticholinergic agents cause bronchodilation through inhibition of vagal stimulation of the airways. The availability of the long-acting anticholinergic agent tiotropium bromide has led to a shift toward using this agent as first-line therapy.
When is continuous supplemental oxygen indicated in COPD?
- In patients with documented persistent hypoxemia (i.e., PaO2 <90%), continuous supplemental oxygen is indicated.
- Patients with signs of cor pulmonale and right heart failure should also receive supplemental oxygen even with less severe hypoxemia.
- Note that oxygen therapy is the only pharmacologic therapy that has been proven to improve survival and quality of life.
What sign related to BP is seen during acute asthma attack?
What breathing pattern is also sometimes observed?
A pulsus paradoxus (an increase in the normal fall in systolic blood pressure [BP] of ≤ 10 mm Hg or less observed during inspiration) can be seen. Severe paradox (≥25 mm Hg) is indicative of a severe attack. Note that as respiratory muscle fatigue develops and the patient can no longer generate increased intrapleural pressure, the paradox can disappear.
Paradoxic breathing pattern (inward movement of the abdominal wall and lower thorax during inspiration)
The development of thrombosis is increased by three major factors (Virchow’s triad):
stasis, alteration in blood vessels (injury), and hypercoagulability
Causes of hypercoagulability (8)
Postpartum period Malignancy Oral contraceptives Deficiencies of protein S, protein C, and antithrombin III Lupus anticoagulant Activated protein C resistance (e.g., factor V Leiden) Prothrombin gene mutations Hyperhomocysteinemia
Most common PE Sx (4)
- most prominent: sudden onset of unexplained dyspnea.
- Pleuritic chest pain (increased with respiration)
- Cough in roughly a third of patients.
- Hemoptysis, although considered a classic finding, is relatively uncommon and usually indicates pulmonary infarction.
PE findings: vitals (3), cardiac and resp exam, other finding
Tachycardia
tachypnea
Low-grade fever (<101°F [38.3°C]) may be encountered
-The pulmonary examination in PE is often completely normal with less than half of all patients presenting with scattered rales as the sole finding.
-Cardiac examination may reveal signs of right-sided heart strain if the embolus is extensive. These include:
Loud pulmonic component of second heart sound (P2), best heard in left second intercostal space
Right-sided S3 (increased with inspiration)
Right ventricular heave (palpable lift over left sternal border)
-maybe Physical findings related to underlying lower extremity thrombosis; seen in only approximately a third of all patients.
